ArticleThe EMBO journal2009
Regulation of heterochromatin remodelling and myogenin expression during muscle differentiation by FAK interaction with MBD2.
Article in The EMBO journal, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 104 citations in OpenAlex.
- Glutamate-induced nuclear translocation of PYK2 in hippocampal neurons, interaction with MBD2, and role in cell death in a model of epilepsy.Cell death & disease · 2026Article
- Heterochromatome wide analyses reveal MBD2 as a phase separation scaffold for heterochromatin compartmentalization and composition.Nucleic acids research · 2025Article
- Versatile functions of methyl-CpG-binding domain 2 (MBD2) in cellular characteristics and differentiation.Molecular biology reports · 2025Review
- FERM domain-containing proteins are active components of the cell nucleus.Life science alliance · 2024Review
- Focal Adhesion Kinase Binds to the HPV E2 Protein to Regulate Initial Replication after Infection.Pathogens (Basel, Switzerland) · 2023Article
- Caspase-mediated nuclear pore complex trimming in cell differentiation and endoplasmic reticulum stress.eLife · 2023Article
- Downregulation of mitochondrial complex I induces ROS production in colorectal cancer subtypes that differently controls migration.Journal of translational medicine · 2023Article
- Simiate and the focal adhesion kinase FAK1 cooperate in the regulation of dendritogenesis.Scientific reports · 2022Article
- New Insights on the Nuclear Functions and Targeting of FAK in Cancer.International journal of molecular sciences · 2022Review
- FAK in Cancer: From Mechanisms to Therapeutic Strategies.International journal of molecular sciences · 2022Review
- Epigenetic modifications in muscle regeneration and progression of Duchenne muscular dystrophy.Clinical epigenetics · 2021Review
- Epigenetic regulation of satellite cell fate during skeletal muscle regeneration.Skeletal muscle · 2021Review
- The Non-receptor Tyrosine Kinase Pyk2 in Brain Function and Neurological and Psychiatric Diseases.Frontiers in synaptic neuroscience · 2021Review
- Direct visualization by FRET-FLIM of a putative mechanosome complex involving Src, Pyk2 and MBD2 in living MLO-Y4 cells.PloS one · 2021Article
- Genetic deletion of microRNA biogenesis in muscle cells reveals a hierarchical non-clustered network that controls focal adhesion signaling during muscle regeneration.Molecular metabolism · 2020Article
- Targeting focal adhesion kinase in cancer cells and the tumor microenvironment.Experimental & molecular medicine · 2020Review
- Nuclear Focal Adhesion Kinase Controls Vascular Smooth Muscle Cell Proliferation and Neointimal Hyperplasia Through GATA4-Mediated Cyclin D1 Transcription.Circulation research · 2019Article
- The roles of nuclear focal adhesion kinase (FAK) on Cancer: a focused review.Journal of experimental & clinical cancer research : CR · 2019Review
- Focal adhesion kinase (FAK) phosphorylation is a key regulator of embryonal rhabdomyosarcoma (ERMS) cell viability and migration.Journal of cancer research and clinical oncology · 2019Article
- Inhibition of FAK Signaling Elicits Lamin A/C-Associated Nuclear Deformity and Cellular Senescence.Frontiers in oncology · 2019Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Focal adhesion kinase (FAK), a major cell adhesion-activated tyrosine kinase, has an important function in cell adhesion and migration. Here, we report a new signalling of FAK in regulating chromatin remodelling by its interaction with MBD2 (methyl CpG-binding protein 2), underlying FAK regulation of myogenin expression and muscle differentiation. FAK interacts with MBD2 in vitro, in myotubes, and in isolated muscle fibres. Such an interaction, increased in myotubes exposed to oxidative stress, enhances FAK nuclear localization. The nuclear FAK-MBD2 complexes alter heterochromatin reorganization and decrease MBD2 association with HDAC1 (histone deacetylase complex 1) and methyl CpG site in the myogenin promoter, thus, inducing myogenin expression. In line with this view are observations that blocking FAK nuclear localization by expressing dominant negative MBD2 or suppression of FAK expression by its miRNA in C2C12 cells attenuates myogenin induction and/or impairs muscle-terminal differentiation. Together, these results suggest an earlier unrecognized role of FAK in regulating chromatin remodelling that is important for myogenin expression and muscle-terminal differentiation, reveal a new mechanism of MBD2 regulation by FAK family tyrosine kinases, and provide a link between cell adhesion and chromatin remodelling.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.